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Administrative data

Link to relevant study record(s)

Description of key information

Short description of key information on bioaccumulation potential result: 
Data available on higher olefins similar to those found in the butylene oligomer category suggest that metabolism occurs in hepatic endoplasmic reticulum via initial formation of a transient epoxide, which is further metabolized to the corresponding glycol or conjugated with glutathione. Following oral or inhalation exposure, these higher olefins can be absorbed into the blood and reach the liver and kidneys.

Key value for chemical safety assessment

Additional information

In accordance with section 1 of REACH Annex XI, testing does not appear to be scientifically necessary since data are available on representative substances which are adequate for the purposes of classification and labelling and/or risk assessment of the butylene oligomers included in this category.

Discussion on bioaccumulation potential result:

Although there are no toxicokinetic data on butylene oligomers, the SIDS Initial Assessment Report on the Higher Olefins – Category details studies with several alpha or internal olefins spanning the range from C6 to C16 which indicate that metabolism occurs in hepatic endoplasmic reticulum via initial formation of a transient epoxide,which is further metabolized to the corresponding glycol or conjugated with glutathione (Watabe and Yamada, 1975; Maynert et al., 1970; Oesch, 1973; Watabe and Maynert, 1968). The latter two metabolites are likely to be excreted in urine as mercapturic acids (Sipes and Gandolfi, 1991).

Effects seen in repeated-dose studies with C6-C8, and C14 alpha olefins and C6, C18 and C20-24 internal olefins indicate that these olefins are absorbed by the blood and reach the liver and kidneys following oral or inhalation exposure. Studies of the toxicokinetic properties of inhaled C2-C10 1 -alkenes confirm that, within the carbon number range tested, absorption occurs and that the alkenes reach the brain, liver, kidneys and perirenal fat, with the concentrations increasing with the number of carbon atoms (Eide et al., 1995; Zahlsen et al., 1993).

Eide I, Hagerman R, Zahlsen K, Tareke E, Tornquist M, Kumar R, Vodicka P and Hemminki K (1995). Uptake, distribution, and formation of hemoglobin and DNA adducts after inhalation of C2 -C8 1-alkenes [olefins] in the rat. Carcinogenesis. 16, 1603 - 1609. Maynert EW, Foreman RL and Watabe T (1970). Epoxides as obligatory intermediates in the metabolism of olefins to glycols. J. Biol. Chem, 245, 5234-5238.

Oesch F (1973). Mammalian epoxide hydrases: inducible enzymes catalysing the inactivation of carcinogenic and cytotoxic metabolites derived from aromatic and olefinic compounds. Xenobiotica 3(5), 305-340.

Sipes IG and Gandolfi AJ (1991). Biotransformation of toxicants. In (1991). Cassarett and Doull’s Toxicology. 4th ed. Edited by Amdur MO, Soull J, and Klassen CD. Pergammon Press, 88-126.

Watabe T and Maynert EW (1968). Pharmacolgist 10,203 as cited in Watabe, T. and N. Yamada (1975). The biotransformation of 1-hexadecene to carcinogenic 1,2-epoxyhexadecane by hepatic microsomes. Biochemical Pharmacology 24, 1051-1053.

Watabe T and Yamada N (1975). The biotransformation of 1-hexadecene to carcinogenic 1,2 -epoxyhexadecane by hepatic microsomes. Biochemical Pharmacology 24, 1051-1053.

Zahlsen K, Eide I, Nilsen AM and Nilsen OG (1993). Inhalation kinetics of C8-C10 1-alkenes and iso-alkanes in the rat after repeated exposures. Pharmacology & Toxicology 73, 163-168.